The periodontal pathogen T. denticola resides in a stressful environment rife with challenges, the human oral cavity. Knowledge of the stress response capabilities of this invasive spirochete is currently very limited. Whole genome expression profiles in response to different suspected stresses including heat shock, osmotic downshift, oxygen and blood exposure were examined. Most of the genes predicted to encode conserved heat shock proteins (HSPs) were found to be induced under heat and oxygen stress. Several of these HSPs also seem to be important for survival in hypotonic solutions and blood. In addition to HSPs, differential regulation of many genes encoding metabolic proteins, hypothetical proteins, transcriptional regulators and transporters was observed in patterns that could betoken functional associations. In summary, stress responses in T. denticola exhibit many similarities to the corresponding stress responses in other organisms but also employ unique components including the induction of hypothetical proteins.

The Treponema denticola cheA gene, encoding the central kinase of the general chemotaxis pathway, was analyzed for its role in chemotaxis and tissue penetration. The cheA gene was interrupted by insertion of an ermF-ermAM gene cassette. Reverse transcription-PCR confirmed that the other downstream chemotaxis genes within the same operon (cheW, cheX, and cheY) were still expressed in the cheA mutant strain. Lack of cheA resulted in decreased swarming on soft-agar swarm plates and failure to respond chemotactically to a mixture of nutrients. Behavioral analyses using video microscopy revealed that the cheA mutant exhibited coordinated cell movement. The cellular reversal frequency, however, was severely reduced, indicating that CheA in T. denticola mainly controls cellular reversal and that active chemotaxis signaling input is not required for coordination of flagellar rotation at both cell poles.